1998 Fiscal Year Final Research Report Summary
Genetic predisposition to hyperthermia-induced seizures and development of excitatory and inhibitory system in the rat brain.
Project/Area Number |
09670812
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pediatrics
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Research Institution | EHIME UNIVERSITY |
Principal Investigator |
MORIMOTO Takehiko Ehime University, School of Medicine, Department of Pediatrics, Assistant Professor, 医学部, 助教授 (40157920)
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Co-Investigator(Kenkyū-buntansha) |
FUKUDA Mitsumasa Ehime University, School of Medicine, Department of Pediatrics, Associate Profes, 医学部, 助手 (80274330)
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Project Period (FY) |
1997 – 1998
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Keywords | neurotransmitter / glutamate / NO / electroencephalography / fever / epilepsy / febrile convulsion / rat / calcium |
Research Abstract |
Fever induces seizures in patients with epilepsy or febrile convulsions. The mechanism for fever-induced seizures has not been elucidated yet. The aim of the present study is to evaluate the neuronal firing in the occipital cortex during hyperthermia and hyperthermia -induced seizures (HS) and to investigate the rote of nitric oxide (NO) in the induction of hvperthermia-induced seizures. Firing frequencies in base line and hyperthermia(maximum cortical temperature 39.7* 1.23 ゚C) were 2.2 (0.0-42.0)(median, range) and 4.0(0.1-68.3) Hz, respectively, indicating significant increase in firing frequency during hyperthermia(p<O.05). Further hyperthermia transformed enhanced neuronal firing into rhythmic burst causing HS.These findings indicate that excitability of the cortex increases with elevation of temperature. NO synthesis was enhanced with hyperthermia and there was a positive corelation between intensity of hyperthermia T(゚C・ second) and release of NO (pA ・second) ; NO=40.7T -390(r=0.69, p<O.O1). Suppression of NO with NO synthetase antagonist elevates the seizure threshold for HS and shorten the seizure duration. These findings indicates that increased NO may contributes to the onset of HS by increasing the neurotransmitter release of neuron in wide area and enhancing the excitability of the brain.
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